Project/Area Number |
22790384
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Experimental pathology
|
Research Institution | University of Miyazaki |
Principal Investigator |
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 遺伝子 / 癌 / 細胞・組織 / 病理学 / 脳神経疾患 |
Research Abstract |
Glioblastoma still remains to be a fatal disease. To identify novel therapeutic targets based on molecular and cell biology regarding malignant features of glioblastoma is purpose of this study. At first, I focused on IGFBP-2 and CD24, both of which were involved in the invasive growth of glioblastoma. The cDNA microarrays for transcriptional profiling revealed significantly reduced expression of progression-associated genes and enhanced expression of suppression-associated genes in response to IGFBP-2 or CD24 knockdown in glioblastoma cell lines. Furthermore, among identified genes as candidates for positive regulators of IGFBP-2, DKK1 and RelA were analyzed. It is revealed that DKK1 is involved in invasiveness not only in glioblastoma, but also pancreatic adenocarcinoma and squamous cell carcinoma. It is also clarified that RelA is involved in the proliferation of glioblastomas, and a RelA inhibitor can suppress the proliferation and tumorigenicity of glioblastoma cells. These genes and the related signal transductions serve as potential therapeutic targets in glioblastoma.
|